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Two-year old seedlings of Silver buffaloberry (Shepherdia argentea (Pursh) Nutt.) were exposed to NaCl salinity (0, 200, 400 and 600 mmol/l) for 30 days. Leaf water potential (Ψ w ), chlorophyll contents (Chl a, b, and a + b) and K + content decreased with an increase in salinity. Relative water content (RWC) declined significantly with 400 and 600 mmol/l NaCl. However, salinity induced an excessive accumulation of Na + in the leaves of plants. Light responses of photosynthesis showed that net photosynthetic rate (P N ) values were continuously raised with the increase of photosynthetic photon flux density (PPFD) at all salinity levels and plants treated with 600 mmol/l salinity suffered from photoinhibition with the lowest P N values. The reduction of P N and stomatal conductance (g s ) associated with a sharp increase of intercellular CO 2 concentration (C i ) in the leaves at 600 mmol/l salt-treated plants showed that non-stomatal limitations might have prevailed over stomatal limitations under severe saline conditions, due to severe cellular dehydration, inhibited synthesis of chlorophyll and ionic imbalance and toxicity. It is concluded that S. argentea possesses high salt tolerance capacity and can be widely cultivated in salt-affected areas.

Numerous studies have found that sucrose (Suc) metabolism plays a crucial role in the environmental stress response of many plant species. The majority of Suc metabolism-associated reports refer to acid invertases (Ac-Invs). However, alkaline/neutral Invs (A/N-Invs) have been poorly studied. In this study, a wheat A/N-Inv gene, Ta-A/N-Inv1, with three copies located on chromosomes 4A, 4B, and 4D, was cloned from a wheat-Puccinia striiformis f. sp. tritici (Pst) interaction cDNA library. Transcripts of the three Ta-A/N-Inv1 copies were up-regulated in wheat leaves that were infected by Pst or had experienced certain abiotic treatments. Furthermore, the expression of Ta-A/N-Inv1 was decreased by treatment with exogenous hormones. Heterologous mutant complementation and subcellular localization revealed that Ta-A/N-Inv1 is a cytoplasmic invertase. Knocking down all three copies of Ta-A/N-Inv1 using the barley stripe mosaic virus-induced gene silencing system reduced the susceptibility of wheat to the Pst virulent pathotype CYR31, which is associated with pathogen-induced H2O2 accumulation and enhanced necrosis. Interestingly, 48h dark treatment of the Ta-A/N-Inv1-knockdown plants immediately after inoculation abrogated their enhanced resistance, suggesting that H2O2 production and its associated cell death and resistance in the Ta-A/N-Inv1-silenced plants require light. Consistent with this observation, photosynthesis and reactive oxygen species (ROS)-related genes were significantly up-regulated in the Ta-A/N-Inv1-knockdown plants infected by CYR31 under light exposure. These results suggest that Ta-A/N-Inv1 might act as a negative regulator in wheat disease resistance to Pst by increasing cytoplasmic hexose accumulation and downregulating photosynthesis of the leaves to avoid cell death due to excessive ROS production.

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